Serum concentrations of asymmetric (ADMA) and symmetric (SDMA) dimethylarginine in patients with chronic kidney diseases

Fleck, Christian; Schweitzer, Frank; Karge, E.; Busch, Martin; Stein, Günter

doi:10.1016/s0009-8981(03)00338-3

Cited by 122 publications

(96 citation statements)

References 79 publications

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“…More recently, the same research group showed that SDMA levels in a large group of patients with renal insufficiency were significantly higher in those who had coronary heart disease or left ventricular hypertrophy compared with those without cardiac comorbidity. 24 In addition, SDMA concentration was increased additionally in all patients with hypertension in comparison with renal patients with normal blood pressure. Thus, although SDMA is not able to directly inhibit NO synthase, it may be of clinical significance by reducing substrate availability of NO synthase through competition with arginine for the y ϩ pump.…”

Section: Discussionmentioning

confidence: 92%

“…However, during renal insufficiency, both dimethylarginines are elevated, and several studies have shown that this increase is more pronounced for SDMA. 8,11,24,25 Interestingly, Fleck and coworkers 11 have shown that SDMA, and not only ADMA, is likely to be responsible for hypertension seen in patients with chronic renal failure. More recently, the same research group showed that SDMA levels in a large group of patients with renal insufficiency were significantly higher in those who had coronary heart disease or left ventricular hypertrophy compared with those without cardiac comorbidity.…”

Section: Discussionmentioning

confidence: 99%

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The human liver clears both asymmetric and symmetric dimethylarginine†

et al. 2005

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Asymmetric (ADMA) and symmetric dimethylarginine (SDMA) inhibit production of nitric oxide. The concentration of both dimethylarginines is regulated by urinary excretion, although ADMA, but not SDMA, is also subject to degradation by dimethylarginine dimethylaminohydrolase, which is highly expressed in the liver but also present in the kidney. The exact roles of the human liver and kidney in the metabolism of dimethylarginines are currently unknown. Therefore, we aimed to investigate renal and hepatic handling of ADMA and SDMA in detail in 24 patients undergoing hepatic surgery. To calculate net organ fluxes and fractional extraction (FE) rates, blood was collected from an arterial line, the portal vein, hepatic vein, and renal vein, and blood flow of the hepatic artery, portal vein, and renal vein was determined using Doppler ultrasound techniques. Results showed a significant net uptake ( . FE rates of ADMA for the liver and kidney were 5.0% (3.5%-7.4%) and 8.4% (1.3%-13.9%), respectively. For SDMA, hepatic and renal FE rates were 3.4% (2.1%-7.5%) and 12.5% (3.6%-16.2%), respectively. In conclusion, this study gives a detailed description of the hepatic and renal elimination of dimethylarginines and shows that the clearing of SDMA is not only confined to the kidney, but the human liver also takes up substantial amounts of SDMA from the portal and systemic circulation. (HEPATOLOGY 2005;41:559-565.)

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Section: Discussionmentioning

confidence: 92%

Section: Discussionmentioning

confidence: 99%

The human liver clears both asymmetric and symmetric dimethylarginine†

et al. 2005

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“…The plasma level of ADMA is increased in patients suffering from chronic kidney diseases (CKDs), because its excretion and degradation are decreased. 1,2 The effect of ADMA on cardiovascular system, along with endothelial dysfunction and endothelial injury, is mainly through NOS-NO pathway, that is, a reduction in the production or effect of NO caused by accumulation of ADMA. [3][4][5] More recently, ADMA levels have been shown to be predictive of cardiovascular diseases (CVD) and all-cause mortality in predominantly nondiabetic CKD, 6 type 1 diabetic patients with diabetic nephropathy, 7 end-stage renal disease (ESRD), 8 and coronary artery disease.…”

Section: Introductionmentioning

confidence: 99%

The differences of asymmetric dimethylarginine removal by different dialysis treatments

Zhang¹,

Liu²,

Liu³

et al. 2010

Renal Failure

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Background: Asymmetric dimethylarginine (ADMA) as a uremia toxin is accumulated in end-stage renal disease (ESRD) patients. Elevated ADMA level has been shown to be predictive of cardiovascular diseases (CVDs) and all-cause mortality in ESRD. Therefore, we investigated the removal of ADMA by different dialysis treatments. Methods: There were 30 each of hemodialysis (HD), hemodiafiltration (HDF), peritoneal dialysis (PD) patients, and healthy volunteers enrolled. The ADMA concentrations in serum, urine, and spent dialysate samples were determined. The urine and spent dialysate volumes were recorded. The ADMA removals by urine and spent dialysate in 1 week were calculated and compared among four groups. It was also analyzed for the correlations between the total removal of ADMA in 1 week and the parameters of age, durance of dialysis, glomerular filtration rate, urine volume, urinal ADMA level, spent dialysate volume, and spent dialysate ADMA level. Results: The serum levels of ADMA in dialysis patients were much higher than in healthy subjects (0.32 ± 0.09 μmol/L), and their 1-week total removals of ADMA were much lower than healthy controls (249.21 ± 57.04 μmol/week) (p-values all were less than 0.01). Among dialysis groups, serum ADMA levels decreased significantly in PD patients compared with HD or HDF patients (1.38 ± 0.30 μmol/L vs. 1.82 ± 0.38 μmol/L and 1.63 ± 0.32 μmol/L, p < 0.01), and the total removal of ADMA diminished remarkably by turns of PD, HDF, and HD groups (47.79 ± 8.20 μmol/week, 31.79 ± 8.92 μmol/week, 14.63 ± 6.53 μmol/week, respectively, p < 0.01). The total removal of ADMA in 1 week was related directly with the spent dialysate concentrations of ADMA, the spent dialysate volume, and the urine volume. Conclusions: ADMA was mainly removed by dialysate in dialysis patients. Different dialysis models have different clearance capability on plasma ADMA. PD might be more effective on ADMA removal than HD and HDF, with HDF being more effective than HD.

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“…Thus, any severe renal insufficiency is liable to lead to increased ADMA blood levels. 70 Interestingly, ADMA molecules produced in the cells of a specific tissue may act and inhibit NO synthase in other tissues. Such a phenomenon is observed between macrophage and endothelial cells 71 and possibly between smooth muscle and endothelial cells.…”

Section: Hormone Therapy and Cardiovascular Diseasementioning

confidence: 99%

Hormone therapy and asymmetrical dimethylarginine in postmenopausal women

Karkanaki

Vavilis

Traianos

et al. 2010

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Women present an estradiol-dependent cardiovascular risk profile. based on various studies, it was considered that estrogen therapy (Et) in postmenopausal women could probably reduce the higher cardiovascular risk in this group. Assymetric dimethylarginine (ADMA) is an endogenous methylated arginine which inhibits nitric oxide (NO) synthesis by competing with the substrate of NO, L-arginine, leading to endothelial dysfunction and, consequently, to atherosclerosis. Moreover, ADMA has been considered as an independent risk factor for cardiovascular disease. It has also been found that hormone therapy (Ht), and mainly oral estrogen therapy, lowers ADMA concentrations in healthy postmenopausal women. the effect of estrogens on ADMA levels, although small, is considered important, as physiological variation of ADMA is limited. Nevertheless, larger randomized trials are necessary to establish that estrogens substantially lower ADMA levels and that these changes really reflect improved cardiovascular prognosis in postmenopausal women.

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Serum concentrations of asymmetric (ADMA) and symmetric (SDMA) dimethylarginine in patients with chronic kidney diseases

Cited by 122 publications

References 79 publications

The human liver clears both asymmetric and symmetric dimethylarginine†

The human liver clears both asymmetric and symmetric dimethylarginine†

The differences of asymmetric dimethylarginine removal by different dialysis treatments

Hormone therapy and asymmetrical dimethylarginine in postmenopausal women

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